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Artykuły w czasopismach na temat "Phénotypiques"
Shabajee, Preety, Albane Gaudeau, Céline Legros, Thierry Dorval i Jean-Philippe Stéphan. "Du criblage à haut contenu à la déconvolution de cibles". médecine/sciences 37, nr 3 (marzec 2021): 249–57. http://dx.doi.org/10.1051/medsci/2021013.
Pełny tekst źródłaSokouri, D. P., N. E. Loukou, C. V. Yapi-Gnaoré, F. Mondeil i F. Gnangbe. "Caractérisation phénotypique des bovins à viande (Bos taurus et Bos indicus) au centre (Bouaké) et au nord (Korhogo) de la Côte d'Ivoire". Animal Genetic Resources Information 40 (kwiecień 2007): 43–53. http://dx.doi.org/10.1017/s1014233900002182.
Pełny tekst źródłaBoujenane, I. "Estimation des paramètres génétiques et phénotypiques de la production laitière des vaches de race Frisonnes Holstein au Maroc". Revue d’élevage et de médecine vétérinaire des pays tropicaux 55, nr 1 (1.01.2002): 63. http://dx.doi.org/10.19182/remvt.9848.
Pełny tekst źródłaNguyen, K., G. Bassez, D. Figarella-Branger, F. Leturcq, B. Eymard, N. Lévy i J. Pouget. "Les dysferlinopathies : aspects phénotypiques et génétiques". Revue Neurologique 160, nr 1 (styczeń 2004): 12. http://dx.doi.org/10.1016/s0035-3787(04)70870-x.
Pełny tekst źródłaNguyen, K., G. Bassez, D. Figarella-Branger, F. Leturcq, B. Eymard, N. Lévy i J. Pouget. "Les dysferlinopathies : aspects phénotypiques et génétiques". Revue Neurologique 160, nr 10 (październik 2004): 975–76. http://dx.doi.org/10.1016/s0035-3787(04)71131-5.
Pełny tekst źródłaCutting, Garry R. "Causes des variations phénotypiques de la mucoviscidose". Annales Nestlé (Ed. française) 64, nr 3 (2006): 111–18. http://dx.doi.org/10.1159/000099044.
Pełny tekst źródłaLudes, B., T. Delabarde i C. Keyser. "Traits phénotypiques et identification génétique des individus". Morphologie 99, nr 326 (wrzesień 2015): 93. http://dx.doi.org/10.1016/j.morpho.2015.07.054.
Pełny tekst źródłaFedala, N. S., M. Kesraoui, N. Belhadj Aissa, A. E. M. Haddam i F. Chentli. "Corrélations phénotypiques et histologiques des masses surrénaliennes". Annales d'Endocrinologie 75, nr 5-6 (październik 2014): 468. http://dx.doi.org/10.1016/j.ando.2014.07.671.
Pełny tekst źródłaMichel, Jean-Baptiste. "William Harvey réinterprété à la lumière de l’évolution des espèces (I)". médecine/sciences 36, nr 11 (listopad 2020): 997–1003. http://dx.doi.org/10.1051/medsci/2020170.
Pełny tekst źródłaLIGOUT, S., i R. H. PORTER. "La reconnaissance sociale chez les mammifères : mécanismes et bases sensorielles impliquées". INRAE Productions Animales 19, nr 2 (13.03.2006): 119–34. http://dx.doi.org/10.20870/productions-animales.2006.19.2.3490.
Pełny tekst źródłaRozprawy doktorskie na temat "Phénotypiques"
Vincent, Levy-Frebault Véronique. "Analyses phénotypiques et génotypiques dans le genre Mycobacterium". Paris 7, 1985. http://www.theses.fr/1985PA077091.
Pełny tekst źródłaSutera, Vivien. "Francisella et antibio-resistance : aspects génétiques, phénotypiques et cliniques". Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV064/document.
Pełny tekst źródłaFrancisella tularensis is a gram-negative facultative intracellular bacterium, causing tularemia. This zoonosis is mainly related to two subspecies: F. tularensis subsp. tularensis (type A) and F. tularensis subsp. holarctica (type B) in North America and throughout the Northern Hemisphere, respectively. Infections with this second subspecies, less virulent than the first one, predominantly induce glandular clinical forms of mild to moderate severity. Their treatment is based on antibiotherapy using a fluoroquinolone or a tetracycline. The use of aminoglycosides is reserved for severe clinical forms. The lymph nodes infection, however, often become chronic (20 to 40% of cases), despite administration of an appropriate antibiotic treatment.The aim of this study was to verify the hypothesis of the emergence of bacterial resistance in Francisella, which could explain treatment failures. It is based on the development and study of an in vitro evolutionary experiment of the bacterium in the presence of ciprofloxacin, a fluoroquinolone. Our work confirmed the bacterium's ability to evolve towards a high-level of resistance to fluoroquinolones, this evolution being correlated with the accumulation of mutations in the genes encoding for type II topoisomerases. In addition, we observed in all strains of F. tularensis subsp. holarctica resistant to fluoroquinolones at a clinically significant level, the presence of mutations altering the GyrA subunit of DNA gyrase at amino acids positions 83 and 87. The research of this marker in clinical samples from patients with treatment failure following appropriate antibiotic treatment was however unsuccessful.After checking the action of antibiotics on bacteria internalized in the intracellular compartment in fibroblast cells, we looked for other mutations induced during the evolution of Francisella to resistance to fluoroquinolones. This study unveiled the involvement of several transmembrane transport systems in antibiotic resistance. We also revealed the existence of a second major target involved in Francisella iron metabolism. The alteration of this target (FupA/B), in addition to being associated with an increase in fluoroquinolone resistance, is correlated with a sharp decrease in the ability of the bacteria to multiply in phagocytic cells
Delhaye, Myriam. "Marqueurs phénotypiques au cours de l'hépatocarcinogénèse expérimentale et humaine". Doctoral thesis, Universite Libre de Bruxelles, 1993. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212869.
Pełny tekst źródłaVergori, Luisa. "Rôle de PPARα sur les modulations phénotypiques des progéniteurs". Angers, 2013. http://www.theses.fr/2013ANGE0045.
Pełny tekst źródłaFort, Patrice. "Rôle de la dystrophine Dp71 dans l'oeil : Impacts phénotypiques". Université Louis Pasteur (Strasbourg) (1971-2008), 2005. https://publication-theses.unistra.fr/public/theses_doctorat/2005/FORT_Patrice_2005.pdf.
Pełny tekst źródłaThe first phenotype to be described among patients suffering from the Duchenne muscular dystrophy (DMD) is the progressive muscular degeneration related to the absence of the hole DMD gene product: the dystrophin. Various work undertaken thereafter led to the description of others troubles among these patients, affecting in particular their cognitive performances in a nonprogressive way. These works also made it possible to show that these affections were particularly related to the DMD gene short products and particularly Dp71. Dp71 is the mainly expressed product of this gene in many tissus among which the central nervous system including the retina. The discovery, in the middle of the 1990’s, that 80% of the DMD patients present a disturbance of the retinal neurotransmission led us to study the role of the dystrophins and in particular Dp71 in the retina using a transgenic mouse in which the expression of this protein was inactivated. This study enabled us to show that this DMD gene product is only expressed by the main glial cells of the retina, the Müller glial cells, where it is only accompanied by the utrophin, the product of an homologous gene of the dystrophin. We have also shown that Dp71 was responsible for the localization of two proteins essential for the homeostasis regulation of the retina: the potassic channel Kir4. 1 and the aqueous channel AQP4. Moreover the absence of Dp71 induce a significant increase in neuronal death following an ischaemic event putting forward the intervention of Dp71 in the regulation of retinal homeostasis. At the time of the clinical study of the defective mouse for the Dp71, we discovered another pathological phenomenon dependent on the absence of this protein: the development of a progressive congenital cataract. Since dystrophins had never been studied in the crystalline lens, we first characterized their expression in this structure and showed that Dp71 is also there the main DMD gene product and that it is mainly expressed in the membrane of the crystalline lens secondary fibers where it colocalize with the β-dystroglycane and the aquaporin channel AQP0. Although complementary studies are necessary, this seems to indicate that it takes part in a macromolecular complex responsible for the conservation of the integrity of the membrane of secondary fibres of the crystalline lens. The whole of this work puts forward the role of Dp71 in the vision, as well in one part of the central nervous system, the retina, as in a very specific epithelial tissue, the crystalline lens
Touch, Sothea. "Cellules immunitaires dans les maladies cardiométaboliques : altérations phénotypiques et fonctionnelles". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066084/document.
Pełny tekst źródłaA common feature between cardiometabolic diseases (CMDs) is a state of chronic low-grade inflammation. In obesity and type-2-diabetes (T2D) notably, insulin resistance has been linked to inflammation in several tissues. The objective of this project is to evaluate the interactions between immune cell alterations and metabolic perturbations in CMDs. In a first study, we investigated intestinal immunity and cytokine production of intestinal T cells in a cohort of lean and obese subjects and evaluated the functional relationship between T cells and enterocytes. We demonstrated that T cell density and cytokine production was increased in the jejunal mucosa of obese subjects and promoted insulin resistance in enterocytes in vitro. In a second study, we characterized mucosal-associated invariant T (MAIT) cells, a subset of T cells recognizing bacterial vitamin B derivatives, in 5 groups of patients with different forms CMDs (metabolic syndrome, obesity, T2D, coronary artery disease with or without heart failure) compared to healthy subjects. We demonstrated that MAIT cell decrease is correlated with HbA1c and is a common feature in all CMD groups. In an ex vivo study, we show that their depletion in the blood could be explained by a higher propensity to apoptosis under high glucose concentrations. Altogether, our findings suggest that the jejunal immune microenvironment could participate in local and systemic metabolic perturbations in human obesity. We also demonstrate that the abundance immune cells, such as circulating MAIT cells could serve as an early marker of cardiometabolic dysfunction
Silva, Nelly Da. "Dépigmentation et dolichomégalie chez une souris : analyses génétiques et phénotypiques". Paris 7, 2002. http://www.theses.fr/2002PA077177.
Pełny tekst źródłaPinaudeau-Nasarre, Cécile. "Stades de spécification de différents aspects phénotypiques de neurones corticaux". Poitiers, 2002. http://www.theses.fr/2002POIT2295.
Pełny tekst źródłaDulac, Amélie. "Marqueurs phénotypiques de la diversité des ressources génétiques du genre Hydrangea". Phd thesis, Université d'Angers, 2011. http://tel.archives-ouvertes.fr/tel-00971779.
Pełny tekst źródłaMeffre, Geneviève. "Différences phénotypiques et fonctionnelles des sous-populations de lymphocytes B d'amygdales". Lyon 1, 1996. http://www.theses.fr/1996LYO1T276.
Pełny tekst źródłaKsiążki na temat "Phénotypiques"
Ernest, FOKAM Paul. Classification de quelques caractères phénotypiques chez le voandzou cultivé au Cameroun. Éditions universitaires européennes, 2022.
Znajdź pełny tekst źródłaPhenotypic Plasticity and Evolution: Causes, Consequences, Controversies. Taylor & Francis Group, 2021.
Znajdź pełny tekst źródłaPfennig, David W. PHENOTYPIC PLASTICITY and EVOLUTION: Contexts Causes Consequences. Taylor & Francis Group, 2021.
Znajdź pełny tekst źródłaReboud, Julien. Des micro-gouttes pour remplacer les souris?: Mise au point d?un format innovant de puces à cellules pour l?analyse phénotypique à haut-contenu. Omniscriptum, 2010.
Znajdź pełny tekst źródłaCzęści książek na temat "Phénotypiques"
Sigal-Zafrani, B., P. Cottu i P. de Cremoux. "Que sait-on des modifications phénotypiques et génotypiques entre tumeur primitive et métastase(s) des cancers du sein ?" W Cancer du sein en situation métastatique, 23–28. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0076-9_3.
Pełny tekst źródłaZuñiga, Jean-Paul. "Les nomenclatures phénotypiques comme langage interimpérial". W Constellations d’Empire, 211–23. Casa de Velázquez, 2023. http://dx.doi.org/10.4000/books.cvz.43858.
Pełny tekst źródłaStreszczenia konferencji na temat "Phénotypiques"
Schulthess, A., Guillerminet, V. Ahossi i F. Denis. "Le syndrome KBG expression phénotypique et odontostomatologique : à propos d’un cas". W 64ème Congrès de la SFCO, redaktorzy S. Boisramé, S. Cousty, J. C. Deschaumes, V. Descroix, L. Devoize, P. Lesclous, C. Mauprivez i T. Fortin. Les Ulis, France: EDP Sciences, 2016. http://dx.doi.org/10.1051/sfco/20166403021.
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